Biomedical subjects

J Cervós-Navarro

Publications and source records attributed to J Cervós-Navarro.

At least 19 recordsLinked to original sources

PubMed1992

Krause's end-bulb microtumor of the conjunctiva: optic and ultrastructural description of a case.

Ultrastructural examination of a conjunctival biopsy of a 90-year-old woman with a history of chronic lymphatic leukemia showed numerous densely packed structures located below the epithelial conjunctival layer. They were composed of concentrical flattened lamellae arranged around one or several clear cores containing a large number of mitochondria. The plasma membranes of the lamellae displayed large numbers of pinocytotic vesicles and resembled perineurial cell processes. The central areas were thought to be axons. Because of their conjunctional location and morphological features. The structures were categorized as nerve endings of the Krause's end-bulb type. The aberrant and profuse growth of these structures led to the diagnosis of Krause's end-bulb microtumor of the conjunctiva. We compare our findings with mucosal neuromas, paraneoplastic lesions and age-related alterations are discussed, although they differ morphologically from Krause's end-bulb microtumor.

Aged↗

PubMed1992

In vivo study of flow pattern at human carotid bifurcation with regard to aneurysm development.

In order to investigate the developmental mechanism of cerebral aneurysms, the in vivo flow pattern around human cervical carotid bifurcations was studied by flow visualization using digital subtraction angiography with an isotonic contrast medium. The blood stream containing the medium impinged on the apex, then proceeded along the walls of the branches. After opacification of the whole lumen around the apex, most of the medium was carried away, while some remained for a few seconds at the carotid sinus. In the internal carotid artery, the blood struck the wall at an oblique angle near the tops of the arterial curvatures. In cases with atheromatous plaque or kinking of the branch, the blood passed through the stenosed segment and moved upstream, indicating turbulence. The study suggests that haemodynamic forces around the apex consist mainly of impingement on the apex and shear stress to the wall at and around the apex. In branches, high shear stress seems to exist. It might be possible that high shear stress causes degenerative changes in the endothelial layer, initiating the formation of saccular and fusiform cerebral aneurysms.

Adolescent↗

PubMed1992

Alterations in cerebral vessels in experimental animals and their possible relationship to the development of aneurysms.

Aneurysmal changes were studied by light and electron microscopes in experimental monkeys to elucidate their pathogenesis. Early changes were found not at the medial defect but in one branch near the apex. Degeneration of the elastic lamina was always more than that of the media throughout the process of aneurysm formation. Endothelial injury was present even at the bifurcation without a bulge. The present study suggests that aneurysmal changes are initiated by degenerative changes in the endothelium, which are followed by alterations in the underlying elastic lamina and, in turn, in the medial layer.

Animals↗

PubMed1992

Acute systemic heat stress increases glial fibrillary acidic protein immunoreactivity in brain: experimental observations in conscious normotensive young rats.

The possibility that astrocytes participate in the pathophysiology of thermal brain injury caused by systemic heat exposure was examined in conscious young rats. The temporal and regional pattern of the astrocytic response to thermal injury was characterized by demonstrating the immunoreactivity of glial fibrillary acidic protein (GFAP) using monoclonal antibody and avidin-biotin complex technique. Exposure of conscious young animals to heat at 38 degrees C for 4 h in a biological oxygen demand incubator resulted in a marked increase of the GFAP immunoreactivity in specific brain regions as compared with the intact controls. The intensity of the increased GFAP immunoreactivity was mainly noted in pons, medulla and cerebellum, followed by thalamus, hypothalamus, hippocampus and caudate nucleus. The cerebral cortex of heat-exposed animals showed only a mild increase in GFAP immunoreactivity which was predominantly concentrated in cingulate, parietal and pyriform cortices. The immunostaining in general was seen in the perivascular glia, within the neuropil and the glia limitans. This increase in GFAP immunoreactivity was absent in animals exposed to the same ambient temperature (38 degrees C) for 1 h and 2 h, or at a lower temperature (36 degrees C) for 4 h. These results show that (i) astrocytes actively participate in the pathophysiology of heat stress, (ii) endogenous thermal brain injury elicits activation and hypertrophy of astrocytes ("reactive gliosis") depending on the magnitude and duration of the ambient heat stimulus, and (iii) the astrocytic reaction (observed as increased GFAP immunostaining) could be induced much more rapidly within a very short survival period of 4 h, not reported earlier.

Animals↗

PubMed1992

Age-related pathophysiology of the blood-brain barrier in heat stress.

The possibility that the blood-brain barrier (BBB) might play an important role in the pathophysiology of heat stress (HS) has been examined in young (age 8-9 weeks) and adult (age 24-32 weeks) rats. Exposure of young rats to 4 h HS at 38 degrees C in a biological oxygen demand (BOD) incubator (relative humidity 47-50%, wind velocity 20-26 cm/sec, simulating the environmental conditions of Varanasi, India, during the month of June) resulted in a marked hyperthermia (41.7 +/- 0.23 degrees C) and behavioral symptoms. In these animals there was a profound increase in the permeability of the BBB to Evans blue-albumin (EBA) (464%) and to 131I-sodium iodide (515%), accompanied by a marked increase in the brain water content (4%), of the levels of serotonin (5-hydroxytryptamine, 5-HT) in plasma (687%) and in brain (267%) and a pronounced reduction (30%) in cerebral blood flow (CBF). Morphological examination using light- and electron-microscopy revealed profound neuronal changes associated with a marked increase in glial fibrillary acidic protein (GFAP) and in vimentin immunoreactivities, together with a substantial reduction in myelin basic protein (MBP) immunostaining in the brain. These changes were more pronounced in the brain-stem reticular formation, pons and medulla region. On the other hand, exposure of adult animals to the same intensity of HS resulted in mild or no changes in BBB permeability, content of brain water and 5-HT in the plasma and brain, CBF or other cellular changes.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1992

Focal involvement and lateralization in Creutzfeldt-Jakob disease: correlation of clinical, electroencephalographic and neuropathological findings.

Focal involvement can be assumed in the initial stage of Creutzfeldt-Jakob disease (CJD). We correlated the clinical, electroencephalographic and neuropathological findings in 13 cases of CJD with special reference to focal or lateralized changes. Eight cases showed clinical and 9 electroencephalographic signs of asymmetry. Four cases with a course of the disease shorter than 12 months presented circumscribed tissue alterations at autopsy. Cases with a clinical duration longer than 12 months had pathological changes involving both hemispheres symmetrically. The infectious agent seems to spread through the entire brain within a period of 12 months.

Adult↗

PubMed1992

Role of serotonin in heat adaptation: an experimental study in the conscious young rat.

The possibility that serotonin may play a role in heat adaptation was examined in a rat model of heat stress (HS). Subjection of animals to acute 4 h HS (but not to 1 h and 2 h duration) in a biological oxygen demand (BOD) incubator (relative humidity 50-55%, wind velocity 20-25 cm/s) resulted in profound hyperthermia (41.68 +/- 0.25 degrees C) associated with behavioural salivation and prostration. This experimental condition simulates the out door environmental conditions of Varanasi, India during the month of June. Measurement of serotonin (5-hydroxytryptamine, 5-HT) content in the plasma and brain showed a profound increase of the amine by 462% and 187% respectively from the control group. Morphological examination in these animals revealed marked cell changes in the brain at both light and electron microscopic level. Thus chromatolysis, shrunken and dark neurons along with a general sponginess of the gray and white matter was quite frequent in all the brain regions. At ultrastructural level, perivascular edema, damage to pre- and postsynaptic terminals, swollen neurons and glial cells, splitting of myelin and vacuolation was very common throughout the whole brain. The microvessels were mainly collapsed and a diffuse infiltration of lanthanum ion within the endothelium was common. Occasionally, lanthanum could also be seen within the basement membrane. However, the tight junctions were mainly intact. On the other hand, when animals exposed to chronic heat stress of 1 h duration at the same intensity for 7 days and then subjected to a 4 h HS on the 8th day, resulted in only minor symptoms. Thus these 4 h heat stressed animals did not exhibit hyperthermia or increased serotonin levels in plasma and brain as compared to the animals exposed to chronic HS of 1 h duration until alone 7th day. These heat adapted animals did not show any marked cell changes in the brain. However, the values of circulating 5-HT level and rectal temperature of these chronically heat stressed animals (for 1 h daily) were mild but significantly elevated on the 7th day as compared to the intact control animals. These results show that: 1. chronic HS of short duration induces heat tolerance; 2. the circulating 5-HT level some how appears to play an important role in the pathophysiology of HS; hand in the physiological mechanism(s) of secondary heat adaptation.

Adaptation, Physiological↗

PubMed1992

Influence of preoperative dexamethasone therapy on proliferating cell nuclear antigen (PCNA) expression in comparison to other parameters in meningiomas.

We conducted a trial in 42 benign and malignant meningiomas to assess a possible influence of preoperative dexamethasone therapy on mitotic index, labelling indices of proliferating cell nuclear antigen (PCNA), progesterone receptor, epidermal growth factor receptor (EGF-R), c-erbB-2 oncoprotein, cathepsin D, gamma-gamma enolase as well as the mean number of silver-stained nucleolar organizer region-associated proteins (AgNORs). Tumors with preceding dexamethasone therapy for more than 1 day display significantly less immunohistochemical staining for PCNA. A correlation between the labelling index of PCNA and the degree of malignancy could not be identified. There was no significant effect of preoperative dexamethasone therapy on the other parameters. Our data suggest that dexamethasone may selectively inhibit the expression of PCNA in the G1/S-phase of the cell cycle. Thus, we emphasize the necessity to heed factors, e.g. dexamethasone, which may affect the expression of proliferating markers.

Adult↗

PubMed1992

Enhancement of nerve fibre regeneration by nucleotides after peripheral nerve crush damage. Electrophysiologic and morphometric investigations.

The effect of nucleotide administration on the regeneration of myelinated nerve fibres following crush injury to the sciatic nerve of the rat was studied using both morphometric and electroneurophysiologic techniques. After a standardized localized crush lesion of the right sciatic nerve, rats were given nucleotides daily at a dosage of 3.0 mg/kg body wt uridine monophosphate (UMP), 2.5 mg/kg body wt cytidine monophosphate (CMP) or 3.0 plus 2.5 mg/kg body wt UMP plus CMP, respectively. Observations were made after 20, 40 and 60 days of nerve regeneration for comparison with age-matched crushed or nonoperated controls. Electroneurophysiologic studies of right sural nerves were performed as single fibre measurements. Morphometry was performed on semithin transverse sections of the right common peroneal nerve with a fully automatic interactive image analysis system. Forty days after crush injury the single fibre conduction velocity of all type II afferents in the UMP/CMP treated group was significantly accelerated. There was a trend (10% greater than or equal to p greater than or equal to 5%) to increase of mean efferent single nerve fibre function at this time. Morphometry of nerve fibres revealed a trend to enlargement of mean fibre area and mean fibre diameter related to increased myelin area and myelin thickness. After 60 days, there was a trend to increase of single fibre conduction velocity of all type II afferents in the UMP/CMP treated group. Automated morphometry revealed a significant increase for the following parameters: fibre area, fibre diameter, myelin area, myelin thickness and axon area.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Combined erbB gene overexpression and decreased H-ras gene expression in human gliomas.

The expression of 15 oncogenes including erbB and H-ras in 18 human glial tumors -10 glioblastomas, 1 astrocytoma grade III-IV, 2 oligodendrogliomas grade III, 2 astrocytomas grade II-III, 1 astrocytoma grade II, 1 oligodendroglioma grade II and 1 oligoastrocytoma grade II--was determined by hybridizing RNA against oncogene probes using the Dot Blot technique. Compared with bovine cerebrum (control), the oncogenes abl, erbA, fms, fos, K-ras, mil, mos, myb, rel, sis, src and yes were expressed equally in both bovine cerebrum and the gliomas. However, the expression of erbB was increased 2-9-fold in all except one glioma, and the expression of H-ras was decreased by the factor 0.3-0.7 in 15 tumors. No obvious correlation was found between tumor histology and changed expression of erbB and/or H-ras or between the grade of malignancy and the expression of any oncogene tested. A connection between erbB and H-ras has been shown by several studies. Our results confirm the relationship between H-ras and erbB. However, the meaning of the H-ras decrease in combination with the erbB elevation has to be clarified.

Animals↗

PubMed1992

Acceleration of nerve and muscle regeneration by administration of nucleotides--electroneurophysiological and morphometrical investigations.

The effect of nucleotide administration on the regeneration of myelinated nerve fibres following crush injury to the sciatic nerve of the rat was studied using morphometric techniques. In addition morphometrical investigations of peroneal and soleal muscles were performed at different times. After a localized crush lesion of the right sciatic nerve, rats were given nucleotides daily at a dosage of 3.0 mg/kg body wt uridine monophosphate (UM), 2.5 mg/kg body wt cytidine monophosphate (CMP) or 3.0 plus 2.5 mg/kg body wt UMP plus CMP, respectively. Observations were made after 20, 40 and 60 days of common peroneal nerve regeneration for comparison with age-matched crushed or nonoperated controls. Forty days after daily UMP/CMP administration the single fibre conduction velocity of all type II afferents was significantly accelerated. There was a trend towards increased mean fibre area related to increased myelin area. Mean diameter of type II muscle fibres was increased. After 60 days, there was a trend to increase of single afferent fibre conduction velocity in the UMP/CMP group. In the same group automated morphometry revealed a significant increase of nerve fibre area, myelin area and axon area. At this time an increase was found of type I and/or type II muscle fibres in all animal groups. The present results suggest that both axons (neurons) and myelin sheaths (Schwann cells) of regenerating nerve fibres and regenerating muscle fibres are influenced by nucleotide administration.

Animals↗

PubMed1992

Increase of survival time in experimental hypoxia by cytidine diphosphate choline.

36 Wistar rats were kept in chronic hypoxic hypoxia of 7 vol % of oxygen in 2 experiments over a period of 6 months, other 36 served as controls. Half of the animals of each group received cytidine diphosphate choline (CDP-choline, citicoline, Somazina; CAS 987-78-0) at a dose of 100 mg/kg body weight in the liquid food. Animals in chronic hypoxia without application of CDP-choline developed pathological symptoms and began to die after 19 to 23 weeks in hypoxia. Rats that received CDP-choline developed less prominent pathological symptoms and died later or remained alive until the end of the experiment. Under conditions of extreme hypoxia CDP-choline exhibited a life-prolonging effect.

Animals↗

PubMed1991

Role of histamine in pathophysiology of heat stress in rats.

Role of histamine in pathophysiology of heat stress (HS) was examined using a pharmacological approach. Subjection of young animals (6-7 wks old) to HS at 38 degrees C for 4 in a B.O.D. incubator resulted in a profound increase in blood-brain barrier (BBB) permeability to Evans blue albumin (EBA) and 131I-sodium by 375% and 478% from the control values respectively. At this time period, the brain water content showed a 3.6% increase from the control. Pretreatment with histamine H2 receptor antagonist cimetidine significantly reduced the extravasation of both the tracers and thwarted the increase of brain water content as compared to the untreated group. On the other hand, pretreatment with histamine H1 antagonist mepyramine failed to reduce these parameters. On the contrary, there was a significantly higher permeation of the tracers in brain along with a greater accumulation of brain water content as compared to the untreated group. These results point out a beneficial effect of histamine H2 receptor antagonists in the pathophysiology of HS.

Animals↗

PubMed1991

The role of microthrombi and microcirculatory factors in localization and evolution of focal cerebral ischemia.

Ischemic cerebral infarction is caused primarily by occlusion of a large arterial vessel. Local circulatory disturbances in the center of ischemic tissue and in ischemic penumbra and the degree of sensitivity to ischemia in different brain regions influence subsequent ischemic progression. Postischemic recirculation is impaired by hemodynamic disturbances and formation of microthrombi, hemorrheologic changes and degeneratively altered vessels of microcirculation. Increased postischemic coagulation can be demonstrated in laboratory tests of few minutes extending up to two weeks after the onset of ischemia. Morphological observations on microthrombi after experimental focal ischemia as well as in patients with cerebral infarction show that formation of microthrombi is dependent on the duration of ischemia and the extent of infarcted tissue. Microthrombi are most prevalent in early stages of tissue damage. This suggests that microthrombi have an effect on the progression of ischemic necrosis. On the basis of our results, we can state that 1) microcirculatory disturbances are triggered by focal cerebral ischemia, 2) formation of microthrombi is a contributing factor to the evolution of postischemic microcirculatory disturbances, and 3) microthrombi promote the progression of ischemic necrosis.

Animals↗

PubMed1991

Spontaneous saccular cerebral aneurysm in a rat.

A saccular cerebral aneurysm was incidentally found at the bifurcation of a fenestrated anterior cerebral artery of 35-week-old Sprague-Dawley rat. The animal had been fed a normal laboratory diet. The internal lamina extended for a short distance into the neck of the aneurysm and then suddenly disappeared. The medial layer ended abruptly at the neck of the aneurysm. The aneurysmal wall consisted mainly of connective tissue, and of some poorly stained fragments of elastic lamina. No evidence of polyarteritis nodosa or any other inflammatory reaction was obtained. These findings were the same as those observed in man. Therefore, this aneurysm proved to be of truly spontaneous origin. In contrast to experimental aneurysms in rats and in monkeys, in which aneurysms are observed very often, degenerative changes of the elastic lamina in spontaneous aneurysm in the rat were confined to the neck of the aneurysm. This fact may explain partly the difference in frequency between spontaneous and experimental aneurysms in animals. The present study indicates that degenerative changes of the elastic lamina play a very important role in the development of saccular cerebral aneurysms.

Animals↗

PubMed1991

Oxalate-induced encephalitis after infusions of sugar surrogates.

The case of a 55-year-old female with oxalate-induced lethal encephalitis following infusions of sugar surrogates is reported. Renal failure and subsequent central coma developed following the use of xylitol, fructose and sorbitol above the recommended dosages. The patient died due to raised intracranial pressure. Cerebral damage was caused by encephalitis due to calcium oxalate crystals. Oxalosis induced by sugar surrogates may be explained either by dose-dependent toxic effects or genetically fixed intolerance.

Biopsy↗

PubMed1991

Traumatic brain injuries: structural changes.

A host of complications and consequences may follow a contusion or other brain injury of any sort. An appreciation of the temporal evolution of the contusion from a microscopic standpoint is useful to a full understanding of the process by which physical force damages the brain and how the brain reacts to this damage. Some disruptions of the blood brain barrier quite early will result in extracellular edema. The microscopic appearance of an edematous area is usually spongy with numerous vacuoles. The neuropil may appear bubbly, and glial cells may be swollen. If edema has been long standing, the vacuoles may be larger and in fact a small cyst may appear in the white matter. If focal cerebral edema is not present for long periods of time and the underlying cause has been corrected, residual fluid and electrolytes are eventually removed, restoring the neuropil to a normal state, leaving no sign of its presence. However, in longer standing lesions, myelin pallor and some reactive gliosis may remain indefinitely. Neurons may show swelling very early and for a short period of time, which gives way to shrinkage, eosinophilia, and nuclear pyknosis. These changes may be observed at the periphery of lesions for as long as 5 or 6 months after the initial event. Before dissolution, nuclear pyknosis may remain in the tissue for many days and possibly longer, and may even become mineralized in situ (ferruginated neurons) to remain for years. In a traumatic lesion, swollen and ballooned axons may be found in and around the contusion but also at great distances from it (diffuse axonal injury). Axonal ballooning may be observed between 24 and 48 h postinjury and may persist wherever found for many years. Selective axonal calcification has been observed in humans as well as in experimental trauma. At about 7-10 days postinjury increased numbers of astroglia probably are present. Over the ensuing weeks and months, and probably years, astrocytes increase in number and in fibrillary appearance, eventually resulting in a glial scar in and about the injured area. It is thought that this reactive gliosis results in restoration of the blood-brain barrier in the damaged area.

Astrocytes↗

PubMed1991

Increased blood-brain barrier permeability following acute short-term swimming exercise in conscious normotensive young rats.

The status of the blood-brain barrier (BBB) was examined following short-term forced swimming (FS) exercise in younger rats (age 8-9 wks, 80-90 g). Subjection of animals to continuous FS for 30 min duration increased the permeability of the BBB to Evans blue albumin (EBA) and 131I-sodium in 5 and 8 brain regions, respectively. Extravasation of the tracers was markedly pronounced in the cerebellum followed by the cerebral cortex. EBA staining was confined mainly to the posterior cingulate cortex, parietal and occipital cortices, whole cerebellar vermis and the mediolateral cerebellar cortices as well as the dorsal surface of the hippocampus. In addition to the above brain regions. BBB permeability to 131I-sodium extended to the caudate nucleus, thalamus and hypothalamus. At this time period, the serotonin (5-hydroxytryptamine, 5-HT) content showed a profound increase in plasma and brain of about 150% and 250% respectively from the control value. Pretreatment with p-CPA (p-chlorophenylalanine, a serotonin synthesis inhibitor) prevented both the increased permeability of the BBB and the rise in plasma and brain 5-HT level. However, prior treatment with cyproheptadine (a 5-HT2 receptor antagonist) prevented the increased permeability alone. The 5-HT level continued to remain high. These results suggest that short-term FS increases BBB permeability in specific brain regions. This increased permeability appears to be mediated through serotonin via 5-HT2 receptors.

Animals↗